|
|
|
| Effect of Roxithromycin on the Proliferation of HaCaT Keratinocytes Induced by IL-22 |
| YANG Jin-yan, GUAN Xiao-yan, CHEN Zhao-hui, et al |
| Department of Dermatology; The Second Affiliated Hospital of Xinjiang Medical University; Urumqi; Xinjiang Urumqi; 830064 |
|
|
|
|
Abstract 【Objective】To explore the inhibition of roxithromycin on the proliferation of HaCaT keratinocyte cells induced by interleukin-22 (IL-22) .【Methods】Firstly, HaCaT cell viability was detected by MTT after cells were cultured with IL-22 at concentrations of 0, 12. 5, 25, 50, 100 and 200 μg/mL for 48h. Secondly, HaCaT cell viability was also detected by MTT after cells were cultured with roxithromycin at concentrations of 0, 10, 20, 40, 80, 160 and 320 μg/mL for 48h. Lastly, experiments were divided into the control group (vehicle treatment) , the model group (100 μg/mL IL-22) and roxithromycin groups at low, medium and high-dose groups (100, 300, 1000 μg/mL+100 μg/mL IL-22, respectively) . The cell viability was measured by MTT methodand expressions of cytokeratin16 (K16) , K17, Bax and Bcl-2 were detected by Western blot.【Results】Cell viability of HaCaT was increased by IL-22 at concentrations of 12. 5, 25, 50 and 100 μg/mL. However, the cell viability was decreased by IL-22 at a concentration of 200 μg/mL. Similarly, cell viability was increased by roxithromycin at concentrations of 10、20 μg/mL, but the cell viability was decreased by roxithromycin at concentrations of 40、80、160、320 μg/mL. Compared to the vehicle control group, while the cell viability of IL-22 treated model group was increased, the expression of K16, K17 and Bcl-2 was up-regulated (P＜0.01) , the expression of Bax was down-regulated. Compared to the model group, the cell viability in low, medium and high-dose of roxithromycin groups was decreased, and the expression of K17 was down-regulated. The expression of Bax was up-regulated (P＜0.01) . The expression of K16 and Bcl-2 was down-regulated in roxithromycin medium and high-dose groups.【Conclusion】Roxithromycin can inhibit IL-22-induced proliferation of HaCaT keratinocyte cells by down-regulating the expression of cytokeratin and regulating the expression of cell apoptotic related proteins.
|
|
Received: 08 March 2017
|
|
|
|
|
|
[1] 卢传坚, 韩凌, 彭燕, 等. 中医药治疗银屑病的相关分子机制研究进展[J]. 中华中医药杂志, 2012, 27(5):1364-1369.
[2] 韩莹, 程欣. 银屑病患者外周血淋巴细胞亚群的研究[J]. 检验医学与临床, 2016, 13(4):545-547.
[3] 刘军麟, 邹循辉, 殷梅. 寻常型银屑病患者IL-22水平的变化及其临床意义[J]. 重庆医学, 2014, 43(21):2809-2810.
[4] 陈庆宁, 王小川, 杜鹏, 等. 阿奇霉素对白细胞介素-22诱导的HaCaT角质形成细胞炎症干预作用[J]. 中国临床药理学杂志, 2016, 32(8):696-699.
[5] 朱晓芳, 林向飞, 刘国华, 等. 紫草素对白介素-22介导永生化角质形成细胞株增殖、迁移及分化的影响[J]. 临床皮肤科杂志, 2014, 43(4):215-218.
[6] Karakawa M, Komine M, Tamaki K, et al. Roxithromycin downregulates production of CTACK/CCL27 and MIP-3alpha/CCL20 from epidermal keratinocytes[J]. Arch Dermatol Res, 2010, 302(10):763-767.
[7] Takahashi H, Hashimoto Y, Ishida-Yamamoto A, et al. Roxithromycin suppresses involucrin expression by modulation of activator protein-1 and nuclear factor-kappaB activities of keratinocytes[J]. J Dermatol Sci, 2005, 39(3):175-182.
[8] 赵一, 胡晋红. 银屑病皮肤过度增殖相关细胞因子研究进展[J]. 免疫学杂志, 2013, 29(1):74-77.
[9] Kvist P H, Svensson L, Hagberg O, et al. Comparison of the effects of vitamin D products in a psoriasis plaque test and a murine psoriasis xenograft model[J]. J Transl Med, 2009, 7(1):107.
[10] Reindl J, Pesek J, Kruger T, et al. Proteomic biomarkers for psoriasis and psoriasis arthritis[J]. J Proteomics, 2016, 140:55-61. |
|
|
|
2017, Vol. 34 
